It is a well known fact of life that exposure to ultraviolet light, especially the UVA component, causes skin disorders such as melanoma and non-melanoma skin cancers. Superficial remedies, such as sunscreens, are effective only to a limited extent. This understanding has led to the investigation of new methods to protect the skin from the photodamaging effects of solar UV radiation, or “photocarcinogenesis” as it is called. In recent years there has been considerable interest in the identification of natural botanicals, such as silymarin, with antioxidant and anti-inflammatory properties, and showing anti-cancer and antimutagenic functionality.
It is in this sense that the medicinal benefits of milk thistle have been the subject of intense research by scientists. Although its value as a medicine for a number of health conditions, including dermatological ones, has been known for over 2,000 years, it is only now that science has begun to seriously look at the role played by milk thistle and “silymarin”, its compound active, in the treatment of skin damage.
In an experiment conducted at Palacky University in Czechoslovakia (1), researchers studied the impact of two components of Silybum marianum (the technical name for milk thistle) as a preventative and treatment intervention for skin damage against exposure to UVA rays. Their findings were positive, as these two components, collectively known as “flavonolignans,” were found to perform a number of functions, including increasing keratinocyte viability in irradiated cells, inhibiting ROS production, and stopping further depletion of keratinocytes. ATP. and GSH that takes place at the intracellular level, and stops the peroxidation of membrane lipids. Furthermore, the activation of the caspase-3 process that initiates UVA exposure is halted and reversed when the two components of Silybum marianum are applied. The general picture that emerges, therefore, is that Silybum marianum is a good candidate to be considered for inhibiting UV damage.
An interesting experiment conducted with mice at the University of Alabama at Birmingham was reported in the March-April 2008 issue of Photochem Photobiology (2). Two observations from this research are of special relevance to us here. One is CD11b+ cells, which are the main source of oxidative stress in UV-irradiated skin, which were inhibited by silymarin. The flavonoid also suppressed the leukocyte infiltration that had been induced by UV exposure. The second important observation is that silymarin not only stops UV damage, but also acts as a preventative measure. Another researcher has gone a step further by identifying yet another inversion that this chemical makes to the action of UV rays: it reduces the volume of cells that produce H2O2 and produce the cytokine interleukin-10, the generation of which is activated by UV rays. (6).
Researchers working in the Department of Pharmaceutical Sciences at the University of Colorado (3) have come to much the same conclusion. Their research has shown a positive effect of silibinin in repairing DNA damage induced by UVB rays. Another experiment conducted at the Department of Dermatology at the University of Alabama has observed the inhibitory effect that the flavonoid has on tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate, mezerein, benzoyl peroxide, and okadaic acid (4 ).
Topical application of Silibinin before or immediately after UV irradiation has been found to inhibit the UV-induced generation of thymine dimer-positive cells in the epidermis (5). This research has also shown that terminal sunburn cell formation that is again induced by UV rays is also inhibited when Silibinin is applied.
Two independent investigations make a strong case that silymarin is a highly effective agent for inhibiting and reversing cancers induced by carcinogens and tumor promoters. In both experiments (7), (8), silibinin has been reported to inhibit cancer-causing cells (ERK1/2 activation) and promote benign cells (JNK1/2, p38), making it an effective agent. effective cancer intervention for cancer.
An article published in the journal “Cancer Research” details another in-depth investigation into the efficacy of silymarin as a potential interventional agent against stage I and stage II tumors (9). The paper reports that milk thistle extract has been found to be especially useful in suppressing stage I tumors and inhibiting edema, hyperplasia, proliferative index and oxidative status that occur due to UV radiation. This same result was reached by an independent group of researchers, who used a different chemical substance to induce skin edema in mice (10).
From previous research being carried out around the world, it can be safely concluded that silymarin is proving very effective in inhibiting UV-induced skin damage, and the day may not be far off. milk thistle to become one of the main ingredients in sunscreen lotions. .
References
Svobodová A, Zdarilová A, Walterová D, and Vostálová J. Flavonolignans from Silybum marianum moderate UVA-induced oxidative damage to HaCaT keratinocytes. J Dermatol Sci. 2007 December; 48(3):213-24. Epub 2007 Aug 3.
Katiyar SK, Meleth S and Sharma SD. Silymarin, a flavonoid from milk thistle (Silybum marianum L.) inhibits UV-induced oxidative stress through CD11b+ cell infiltration in mouse skin. Photobiol photochemistry. 2008 Mar-Apr;84(2):266-71. Epub 2007 Nov 28.
Singh RP and Agarwal R. Mechanisms and preclinical efficacy of silibinin in the prevention of skin cancer. Eur J Cancer. September 2005; 41(13):1969-79.
Katiyar SK. Silymarin and skin cancer prevention: anti-inflammatory, antioxidant and immunomodulatory effects. Int J Oncol. 2005 January; 26(1): 169-76.
Dhanalakshmi S, Mallikarjuna GU, Singh RP, and Agarwal R. Silibinin prevents skin damage caused by ultraviolet radiation in SKH-1 hairless mice through a decrease in thymine dimer-positive cells and an upregulation of p53 -p21/Cip1 in the epidermis. Carcinogenesis. 2004 August; 25(8):1459-65. Epub 2004 Mar 19.
Katiyar SK. Silymarin treatment, a plant flavonoid, prevents ultraviolet light-induced immune suppression and oxidative stress in mouse skin. Int J Oncol. December 2002; 21(6):1213-22.
Singh RP, Tyagi AK, Zhao J, and Agarwal R. Silymarin inhibits the growth and causes regression of established skin tumors in SENCAR mice through modulation of mitogen-activated protein kinases and induction of apoptosis. Carcinogenesis. 2002 March; 23(3):499-510.
Jifu Zhao, Moushumi Lahiri-Chatterjee, Yogesh Sharma, and Rajesh Agarwal. Inhibitory effect of a flavonoid antioxidant, silymarin, on benzoyl peroxide-induced tumor promotion, oxidative stress, and inflammatory responses in the skin of SENCAR mice. Carcinogenesis, vol. 21, No. 4, 811-816, April 2000.
Lahiri-Chatterjee M, Katiyar SK, Mohan RR, and Agarwal R. A flavonoid antioxidant, silymarin, provides exceptionally high protection against tumor promotion in the SENCAR mouse skin tumorigenesis model. Cancer Res. February 1, 1999; 59(3):622-32.
Zhao J, Sharma Y, and Agarwal R. Significant inhibition by the antioxidant flavonoid silymarin against 12-O-tetradecanoylphorbol 13-acetate modulation of antioxidant and inflammatory enzymes, and expression of cyclooxygenase-2 and interleukin-1-alpha in SENCAR epidermis mouse: implications in preventing the production of stage I tumors. Mol Carcinog. December 1999; 26(4):321-33.